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Epigenetic tumor suppression by BRCA1

Nature Medicine volume 17, pages 1183–1185 (2011)Cite this article

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BRCA1 germline mutations lead to an increased risk of breast and ovarian cancer, but the mechanisms by which the product of this gene functions as a tumor suppressor have remained elusive. Now, analysis of a missense BRCA1 variant shows that it can epigenetically regulate an miRNA implicated in cancer, providing new mechanistic insights (pages 1275–1282).

Women with a family history of breast and/or ovarian cancer have plenty of reasons to undergo genetic testing for mutations in BRCA1, as it is the major locus for predisposition to these cancers, and inactivating germline mutations are present in ∼40% of families with multiple cases of breast cancer1. BRCA1 is involved in a number of cellular processes, such as DNA damage repair, transcriptional regulation and control of cell cycle progression2. BRCA1-linked breast cancers tend to have early onset and be negative for estrogen, progesterone receptors and HER2neu. These 'triple-negative' tumors are particularly difficult to treat3. Moreover, response to DNA-damaging therapy is highly influenced by the BRCA1 status of the tumors3. Thus, BRCA1 mutation carriers can benefit from prophylactic methods as well as from customized treatment options.

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Figure 1: BRCA1 can act as a tumor suppressor by epigenetically regulating the expression of the oncogenic miRNA-155.

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Authors and Affiliations

  1. Aneliya Velkova and Alvaro N.A. Monteiro are at the Cancer Epidemiology Program at H. Lee Moffitt Cancer Center, Tampa, Florida, USA.,

    Aneliya Velkova & Alvaro N A Monteiro

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  1. Aneliya Velkova
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  2. Alvaro N A Monteiro
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Correspondence to Alvaro N A Monteiro.

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The authors declare no competing financial interests.

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Velkova, A., Monteiro, A. Epigenetic tumor suppression by BRCA1. Nat Med 17, 1183–1185 (2011). https://doi.org/10.1038/nm.2493

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